THE CONTROL OF THE RESPIRATION 379 



center, but also because it helps us to explain the nature of the altera- 

 tions which occur in the acid-base equilibrium of the body in all condi- 

 tions which tend to bring about anoxemia. The immediate increase in 

 breathing is the first of the symptoms which demands attention. Ob- 

 viously it cannot be due to the excitation of the respiratory center by an 

 increase in the free C0 2 of the arterial blood (see page 366). Two possi- 

 bilities remain either the reduction of free oxygen in the blood per se 

 excites the center, or this reduction in oxygen causes incompletely oxi- 

 dized acid substances such as lactic acid to appear in the blood so 

 as to raise C H . A clue as to which of these causes is responsible is fur- 

 nished by observation of the C0 2 tension of the alveolar air. It will be 

 recalled that this does not change when the barometric pressure is 

 slightly altered (page 373), but it is otherwise when the reduction is 

 extreme; a progressive decrease occurs. Thus, in one of the experiments, 

 the alveolar C0 2 tension to start with was 40.7 mm. Hg. After lowering 

 the barometric pressure to about 500 mm., the alveolar tensions were : after 

 25 minutes, 36 mm. ; after 90 minutes, 36.8 mm. ; after 175 minutes, 25.7 ; 

 after 465 minutes, 34.9 mm. This shows clearly that increase of free C(X 

 in the blood cannot be the cause for the hyperpnea. Further evidence for 

 this conclusion is afforded by the fact that the breathing after some time 

 returned towards the normal although the alveolar C0 2 tension remained 

 low. 



Increase in C H of the arterial blood on account of the appearance of 

 unoxidized acids, has been considered as the possible cause for the symp- 

 toms of anoxemia. This hypothesis demands close attention because it 

 has been very widely accepted and has seemed to be supported by nu- 

 merous observations, both physiological and clinical. Physiologists, 

 for example, have known for long that lactic acid accumulates in the 

 blood and appears in the urine in all conditions in which there is de- 

 ficient oxidation in the tissues. Thus, Araki found it in the urine after 

 asphyxia produced either by obstruction to breathing or by inspiring 

 coal gas. Hopkins and Fletcher showed that it appears in muscle when- 

 ever this is made to contract in deficiency of oxygen, and Ryffle found 

 it increased in the blood and was present in the urine excreted after vigor- 

 ous muscular exercise. From the clinical side the evidence has been fur- 

 nished by observing the behavior of patients suffering from acidosis 

 due to the appearance of oxybutyric acid (page 737), as in diabetes, or 

 of other acids, as in certain cases of nephritis. In these cases hyperp- 

 nea is accompanied by a lowered tension of alveolar C0 2 and by a lowered 

 capacity of the blood to combine with C0 2 , that is a lowered alkaline 

 reserve (page 38). If the alkaline reserve of the blood be determined 

 after exposure of an animal (man) to low oxygen, it has also been found 

 to be decreased. 



